![]() ![]() Is maintaining good health potentially compatible with a significant or radical life extension? Historically, these phenomena have often been seen as conflicting. Lastly, we hypothesize that transitions are generally small and slow during ageing and more dynamic in disease emergence or progression, with both cases being characterized by system-wide changes in the expression and function of their components, the topology of their interactions, and the system’s overall robustness. We also review the genomic, methylomic, transcriptomic and metabolomic changes that accumulate with age, and discuss them as potential drivers of shifts towards pathological phenotypes. In this chapter, we discuss how differences in heritable components, repair mechanisms, and exposure to events in early or adult life, influence healthspan, longevity and susceptibility to pathologies. On the molecular level, states depend on the combined effect of a myriad of genetic, epigenetic and environmental factors, and in response to a time-varying signal from the exposome, the system may transit between states of health, states with better or worse fitness, and disorder states. However, keeping homeostasis requires parameters dynamically fluctuating within a physiological range. Depending on how flexible the definition of a state is, systems may have multiple healthy and stable states. Health and pathologies are multifactorial states characterizing how well biological systems function in a range of conditions and facing various stressors. ![]()
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